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实验性贫血对虹鳟鱼体外 CO2 排泄的影响。

The effects of experimental anaemia on CO2 excretionin vitro in rainbow trout,Oncorhynchus mykiss.

机构信息

Department of Biology, University of Ottawa, 30 Marie Curie, K1N 6N5, Ottawa, Canada,

出版信息

Fish Physiol Biochem. 1996 Feb;15(1):83-94. doi: 10.1007/BF01874841.

Abstract

The effects of severe experimental anaemia on red blood cell HCO3 (-) dehydrationin vitro were examined in rainbow trout,Oncorhynchus mykiss. After 5 days of anaemia (haematocrit=4.9±1.1%) induced by intraperitoneal injection of phenylhydrazine hydrochloride, fish displayed elevated arterial CO2 tensions (anaemic PaCO2=3.19±0.42 torrvs. control PaCO2=1.35±0.17 torr) and a significant acidosis (anaemic pHa=7.73±0.04vs. control pHa=7.99±0.04). However, after 15-20 days of anaemia (hct=6.6±0.8%) induced by blood withdrawal, the arterial CO2 tension was significantly lower than the control value, suggesting that physiological adjustments occurred within this time period to compensate for the lowered haematocrit. Compensation probably did not involve alterations in ventilation, which was unaffected by 5 days of anaemia (anaemic[Formula: see text];w=786±187 ml min(-1) kg(-1) vs. control[Formula: see text];w=945±175 min(-1) kg(-1)), based on indirect Fick principle measurements.Potential adaptations to longer term anaemia at the level of the red blood cells were investigated using a radioisotopic HCO3 (-) dehydration assay. Owing to the difference in haematocrits, the HCO3 (-) dehydration rate for blood from anaemic fish was significantly lower than that for control fish following equilibration at the same CO2 tension. This difference was eliminated when HCO3 (-) dehydration rates were measured on blood samples adjusted to the same haematocrit, a result which implies that the intrinsic rate of CO2 excretion at the level of the red blood cell was not 'up-regulated' during anaemia. The difference was also eliminated by equilibrating the blood samples with CO2 tensions appropriate for the group from which the sample was obtained,i.e., PCO2=1.4 torr for control samples and PCO2=3.2 torr for anaemic samples; each at the appropriate haematocrit. It is concluded that the elevated PaCO2 helps to reset CO2 excretion to the control level, but that some additional physiological adjustment occurs to lower the PaCO2 after 15-20 days of anaemia.

摘要

本研究旨在探究严重实验性贫血对虹鳟鱼红细胞 HCO3(-)脱水的影响。虹鳟鱼经腹腔注射盐酸苯肼 5 天后,出现贫血(血细胞比容=4.9±1.1%),动脉血二氧化碳张力升高(贫血 PaCO2=3.19±0.42 托 vs. 对照 PaCO2=1.35±0.17 托),酸中毒明显(贫血 pHa=7.73±0.04 vs. 对照 pHa=7.99±0.04)。然而,经静脉采血 15-20 天后,贫血(血细胞比容=6.6±0.8%)导致的动脉血二氧化碳张力显著低于对照值,表明在此期间发生了生理调节以代偿降低的血细胞比容。代偿可能不涉及通气的改变,因为 5 天的贫血对通气没有影响(贫血[公式:见正文];w=786±187 ml min(-1)kg(-1) vs. 对照[公式:见正文];w=945±175 min(-1)kg(-1)),基于间接 Fick 原理测量。为了研究红细胞水平对长期贫血的潜在适应,本研究采用放射性同位素 HCO3(-)脱水测定法。由于血细胞比容的差异,在相同 CO2 张力下平衡后,贫血鱼的血液 HCO3(-)脱水率明显低于对照鱼。当将血液样本调整至相同血细胞比容时,测量 HCO3(-)脱水率,消除了这一差异,这意味着在贫血期间,红细胞水平的 CO2 排泄固有率并未“上调”。当将血液样本与样本来源组的 CO2 张力平衡时,也消除了这一差异,即对照样本的 PCO2=1.4 托,贫血样本的 PCO2=3.2 托;每个样本均在适当的血细胞比容下。结论是,升高的 PaCO2 有助于将 CO2 排泄重置为对照水平,但在贫血 15-20 天后,还会发生一些其他的生理调节以降低 PaCO2。

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